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CCAAT/enhancer-binding protein beta (C/EBPモ) is an important mediator of 1,25 dihydroxyvitamin D3 (1,25D3)-induced receptor activator of nuclear factor kappa-B ligand (RANKL) expression in osteoblasts
Sungsin Jo1, Yun Young Lee2, Jinil Han3, Young Lim Lee1, Subin Yoon1,4, Jaehyun Lee1,4, Younseo Oh1, Joong-Soo Han5, Il-Hoon Sung6, Ye-Soo Park7,#, Tae Hwan Kim1,*,#
1Hanyang University Hospital for Rheumatic Diseases,
2Biomedical Sciences, Graduate School of Biomedical Science and Engineering, Hanyang University,
3Gencurix, Inc,
4Translational Medicine, Graduate School of Biomedical Science and Engineering, Hanyang University,
5Biochemistry and Molecular Biology, Biomedical Research Institute and College of Medicine, Hanyang University,
6Orthopedic Surgery, Hanyang University Seoul Hospital,
7Orthopedic Surgery, Hanyang University Guri Hospital
Receptor activator of nuclear factor kappa B ligand (RANKL) expression in osteoblasts is regulated by 1,25-dihydroxyvitamin D3 (1,25D3). CCAAT/enhancer-binding protein beta (C/EBPモ) has been proposed to function as a transcription factor and upregulate RANKL expression, but it is still uncertain how C/EBPモ is involved in 1,25D3-induced RANKL expression of osteoblasts. 1,25D3 stimulation increased the expression of RANKL and C/EPBモ genes in osteoblasts and enhanced phosphorylation and stability of these proteins. Moreover, induction of RANKL expression by 1,25D3 in osteoblasts was downregulated upon knockdown of C/EBPモ. In contrast, C/EBPモ overexpression directly upregulated RANKL promoter activity and exhibited a synergistic effect on 1,25D3-induced RANKL expression. In particular, 1,25D3 treatment of osteoblasts increased C/EBPモ protein binding to the RANKL promoter. In conclusion, C/EBPモ is required for induction of RANKL by 1,25D3.
Abstract, Accepted Manuscript(in press) [Submitted on July 20, 2018, Accepted on October 10, 2018]
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